About: Genetic Manipulation of Human Intestinal Enteroids Demonstrates the Necessity of a Functional Fucosyltransferase 2 Gene for Secretor-Dependent Human Norovirus Infection

Facets (new session)
Description
Metadata
Settings
- owl:sameAs
- Inference Rule:

About: Genetic Manipulation of Human Intestinal Enteroids Demonstrates the Necessity of a Functional Fucosyltransferase 2 Gene for Secretor-Dependent Human Norovirus Infection Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Genetic Manipulation of Human Intestinal Enteroids Demonstrates the Necessity of a Functional Fucosyltransferase 2 Gene for Secretor-Dependent Human Norovirus Infection
Creator	Ramani, Sasirekha Haga, Kei Atmar, Robert Estes, Mary Griffin, Diane Hopkins, Johns Zeng, Bv, Ayyar Ettayebi, Khalil Fh, Neill Karandikar, Umesh Larson, Göran Lewis, Miranda Lin, Shih-Ching Ma, Lewis Neill, Frederick Tenge, Victoria Uc, Karandikar Vijayalakshmi Ayyar, B Vr, Tenge Zeng, Xi-Lei
Source	Medline; PMC
abstract	Human noroviruses (HuNoVs) are the leading cause of nonbacterial gastroenteritis worldwide. Histo-blood group antigen (HBGA) expression is an important susceptibility factor for HuNoV infection based on controlled human infection models and epidemiologic studies that show an association of secretor status with infection caused by several genotypes. The fucosyltransferase 2 gene (FUT2) affects HBGA expression in intestinal epithelial cells; secretors express a functional FUT2 enzyme, while nonsecretors lack this enzyme and are highly resistant to infection and gastroenteritis caused by many HuNoV strains. These epidemiologic associations are confirmed by infections in stem cell-derived human intestinal enteroid (HIE) cultures. GII.4 HuNoV does not replicate in HIE cultures derived from nonsecretor individuals, while HIEs from secretors are permissive to infection. However, whether FUT2 expression alone is critical for infection remains unproven, since routinely used secretor-positive transformed cell lines are resistant to HuNoV replication. To evaluate the role of FUT2 in HuNoV replication, we used CRISPR or overexpression to genetically manipulate FUT2 gene function to produce isogenic HIE lines with or without FUT2 expression. We show that FUT2 expression alone affects both HuNoV binding to the HIE cell surface and susceptibility to HuNoV infection. These findings indicate that initial binding to a molecule(s) glycosylated by FUT2 is critical for HuNoV infection and that the HuNoV receptor is present in nonsecretor HIEs. In addition to HuNoV studies, these isogenic HIE lines will be useful tools to study other enteric microbes where infection and/or disease outcome is associated with secretor status.
has issue date	2020-03-17(xsd:dateTime)
bibo:doi	10.1128/mbio.00251-20
bibo:pmid	32184242
has license	cc-by
sha1sum (hex)	ee9f3b40ce596b8972c02f7738af62d1191e5290
schema:url	https://doi.org/10.1128/mbio.00251-20
resource representing a document's title	Genetic Manipulation of Human Intestinal Enteroids Demonstrates the Necessity of a Functional Fucosyltransferase 2 Gene for Secretor-Dependent Human Norovirus Infection
has PubMed Central identifier	PMC7078471
has PubMed identifier	32184242
schema:publication	mBio
resource representing a document's body	covid:ee9f3b40ce596b8972c02f7738af62d1191e5290#body_text
is schema:about of	named entity 'human' named entity 'isogenic' named entity 'group' named entity 'FUT2' named entity 'receptor' named entity 'replicate' named entity 'enzyme' named entity 'infection' named entity 'models' named entity 'FUNCTIONAL' named entity 'WHERE' named entity 'GENE FUNCTION' named entity 'CAUSE' named entity 'FACTOR' named entity 'REPLICATION' named entity 'INFECTIONS' named entity 'FUNCTIONAL' named entity 'replication' named entity 'evaluate' named entity 'FUT2' named entity 'FUT2' named entity 'gastroenteritis' named entity 'cell lines' named entity 'epidemiologic' named entity 'individuals' named entity 'produce' named entity 'cell' named entity 'transformed' named entity 'binding' named entity 'antigen' named entity 'replication' named entity 'resistant' named entity 'epidemiologic studies' named entity 'disease' named entity 'enzyme' named entity 'microbes' named entity 'HBGA' named entity 'cell lines' named entity 'infection' named entity 'isogenic' named entity 'CRISPR' named entity 'gastroenteritis' named entity 'epidemiologic' named entity 'FUT2' named entity 'FUT2' named entity 'Fucosyltransferase' named entity 'Infection' named entity 'wild type' named entity 'fucosylation' named entity 'IRES' named entity 'Plasmid' named entity 'infection' named entity 'gene' named entity 'isogenic' named entity 'glycosylation' named entity 'virus infection' named entity 'glycans' named entity 'RNA' named entity 'fucose' named entity 'Cas9' named entity 'recessive mutation'

Faceted Search & Find service v1.13.91 as of Mar 24 2020

Alternative Linked Data Documents: Sponger | ODE Content Formats:

RDF

ODATA

Microdata

About

OpenLink Virtuoso version 07.20.3229 as of Jul 10 2020, on Linux (x86_64-pc-linux-gnu), Single-Server Edition (94 GB total memory)
Data on this page belongs to its respective rights holders.
Virtuoso Faceted Browser Copyright © 2009-2025 OpenLink Software